The Journal of Experimental Medicine
Keystone Symposia
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Published online April 14, 2008
doi:10.1084/jem.20072528
The Journal of Experimental Medicine, Vol. 205, No. 5, 1037-1048
The Rockefeller University Press, 0022-1007 $30.00
© 2008 Fang et al.
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ARTICLE

 Essential role of TNF receptor superfamily 25 (TNFRSF25) in the development of allergic lung inflammation

Lei Fang, Becky Adkins, Vadim Deyev, and Eckhard R. Podack

Department of Microbiology and Immunology, Leonard Miller School of Medicine, University of Miami, Miami, FL 33136

CORRESPONDENCE Eckhard R. Podack: epodack{at}miami.edu

We identify the tumor necrosis factor receptor superfamily 25 (TNFRSF25)/TNFSF15 pair as critical trigger for allergic lung inflammation, which is a cardinal feature of asthma. TNFRSF25 (TNFR25) signals are required to exert T helper cell 2 (Th2) effector function in Th2-polarized CD4 cells and co-stimulate interleukin (IL)-13 production by glycosphingolipid-activated NKT cells. In vivo, antibody blockade of TNFSF15 (TL1A), which is the ligand for TNFR25, inhibits lung inflammation and production of Th2 cytokines such as IL-13, even when administered days after airway antigen exposure. Similarly, blockade of TNFR25 by a dominant-negative (DN) transgene, DN TNFR25, confers resistance to lung inflammation in mice. Allergic lung inflammation–resistant, NKT-deficient mice become susceptible upon adoptive transfer of wild-type NKT cells, but not after transfer of DN TNFR25 transgenic NKT cells. The TNFR25/TL1A pair appears to provide an early signal for Th2 cytokine production in the lung, and therefore may be a drug target in attempts to attenuate lung inflammation in asthmatics.

Abbreviations used: HE, hematoxylin and eosin; PAS, periodic acid-Schiff; tg, transgenic; TNFRSF, TNF receptor superfamily.


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